Tooth decay is caused by demineralization of the tooth structure at either the enamel or root surface. The enamel is a thin layer (1–2 mm) composed of a crystal-type structure of hydroxyapatite or calcium phosphate hydroxide, containing large amounts of calcium and phosphorus. Dental enamel is a porous material and although it contains about 96% by weight of mineral, this is equivalent to approximately 85 percent by volume. The remaining 15 percent by volume is made up of water, protein and lipid, which form the diffusion channels through which acids and minerals can travel into or out of the tooth. The dentin, the major part of the core of the tooth, is composed of CaCO3, a chalk-like material. Although it is 70% by weight of mineral, it also contains 20% by weight organic and 10% by weight water. This corresponds to 47% by volume mineral.
Tooth decay, or dental caries results from the growth of bacteria on the tooth. The bacteria metabolize sugars to acid which can dissolve the tooth. The bacteria grow as a plaque on the tooth and conventional treatment involves periodic removal of the plaque and strengthening of the tooth to make it more resistant to the acid produced by the bacteria.
The majority of tooth decay occurs in the occlusal and unexposed surfaces of the tooth. The tooth is composed of the lingual (back), buccal (front), and occlusal (top) surfaces. The lingual and buccal surfaces are considered to be “flat” although there are grooves and fissures. The occlusal surface is very uneven, composed of pits, fissures, and protuberances. Because of the way the teeth are formed in the mouth, there are also unexposed surfaces of the tooth, such as subgingival surfaces, interproximal surfaces, and contact surfaces.
Methods to prevent tooth decay have typically concentrated on the buccal and lingual surfaces. Unexposed surfaces are usually not treated. Sealants are consistently used on the occlusal surfaces because other methods are relatively ineffective on the occlusal surfaces due to the very different structure and composition of the occlusal surface. The differences include a harder and more fissured surface, the enamel is generally thicker and the structure possesses a different angulation of prisms. In addition, fluoride has previously been shown to be ineffective on the occlusal surface.
Common professional methods to prevent tooth decay have included fluoride, pit and fissure sealants, and varnishes. However, none of these methods individually protect all of the tooth surfaces nor are they permanent, usually lasting less than 5 years. In addition, heat treatment has been explored as an alternative method. By treating the tooth with a very high heat, from 250–1000° C., the structure of the tooth is changed, making it more resistant to acid. This method has never been used clinically because of safety concerns. Because most of the changes to the tooth occur at a very high heat, 1200° C., some changes occur between 500° C. and 1000° C. and a few were seen at temperatures as low as 250° C. to 400° C., there is the potential for thermal damage to the underlying pulpal tissue, adjacent soft tissue and osseous structures. Therefore, although the effects of laser irradiation on dental caries and tooth structure were explored some 30 years ago, the risk of thermal damage to the adjacent hard tissue and pulp was such that much of the research was abandoned. Several laser wavelengths have been explored, including CO2 and Nd:YAG, but both produce a significant amount of heat on the surface of the tooth and in the pulp and provide only a shallow treatment of the tooth itself. With improved laser technology, a number of different types of lasers with varying tissue penetration and energy levels have been developed.
The structural changes produced during the application of heat by CO2 and Nd:YAG lasers at these very high heats include a change in the phosphate molecule in the hydroxyapatite. This makes the tooth less soluble and increases resistance to decay. However, the level of heat produced by these lasers has not been used clinically because it has been shown to damage the tooth structure itself as well as potentially damaging soft tissue.
The action of the laser, as well as other types of tooth treatments, to produce resistance of the tooth to acid can be envisioned as follows: it has been hypothesized that tooth enamel crystals (“hydroxyapatite”) possess two types of sites from which dissolution can occur. The first type of site (the “thermal” site) is less resistant to dissolution by acids under conditions typically found in the oral environment than is the second type of site (the “chemical” site). The treatment of tooth enamel by carbon dioxide laser irradiation or by high temperatures eliminates or reduces the thermal sites, leaving only the chemical sites for dissolution to occur. Once the thermal sites have been eliminated, the tooth enamel is then treated to eliminate the chemical sites with dissolution rate inhibitors or chemical agents. However, even if such laser treatments were clinically usable for safety reasons, they have the disadvantage that they produce only a surface treatment and cannot protect all of the tooth structure, particularly the occlusal and unexposed surfaces.
Therefore, all of these methods are rendered undesirable by that fact that they can only provide temporary treatment, act only at a very shallow depth of the tooth at the lingual and buccal surfaces, and some cannot be used due to safety issues. In addition, none of the above methods can be used in a non-professional setting.